The Impact of Traumatic Brain Injury on the Receipt of Services Following Release from Prison

Traumatic brain injury (TBI) is found at substantially higher rates among incarcerated individuals compared to the general adult population. Individuals with TBI report a higher likelihood to experience a range of deleterious outcomes including substance abuse, depression, post-traumatic stress disorder, aggressive behavior, and violence. Thus, a history of TBI is likely to lead to the types of behaviors that will significantly increase the odds of an individual returning to incarceration post-release, as supported by recent research with a cohort of state prisoners. TBI has largely gone unaddressed by prison reentry programs that are integral to rehabilitating individuals returning to the community. Relatively little is known, however, about the effects of TBI on the receipt of services post-release. Additionally, few studies have examined sex differences in the prevalence of TBI in reentry populations. This chapter uses data from a multi-state prisoner reentry program randomized control trial to examine whether individuals with TBI are significantly different than their peers without TBI with respect to a variety of demographic and psychological metrics and in expressions of needs for and participation in services and programming during the transition from incarceration to the community

Sphingosine-1-phosphate attenuates proteoglycan aggrecan expression via production of prostaglandin E(2 )from human articular chondrocytes

BACKGROUND: Sphingosine-1-phosphate (S1P), a downstream metabolite of ceramide, induces various bioactivities via two distinct pathways: as an intracellular second messenger or through receptor activation. The receptor for S1P (S1PR) is the family of Endothelial differentiation, sphingolipid G-protein-coupled receptor (EDG). We have here attempted to reveal the expression of EDG/S1PR in human articular chondrocytes (HAC), exploring the implications of S1P in cartilage degradation. METHODS: Articular cartilage specimens were obtained from patients with rheumatoid arthritis (RA), osteoarthritis (OA) or traumatic fracture (representing normal chondrocytes) who underwent joint surgery. Isolated HAC were cultured in vitro by monolayer and stimulated with S1P in the presence or absence of inhibitors of signaling molecules. Stimulated cells and culture supernatants were collected and subjected to analyses using reverse transcription-polymerase chain reaction (RT-PCR), Western blotting, and enzyme-linked immunosorbent assay (ELISA). RESULTS: All of the tested HAC samples showed positive results in terms of EDG/S1PR expression in basal condition. When HAC was stimulated with S1P, a significant increase in prostaglandin (PG) E(2 )production was observed together with enhanced expression of cyclooxygenase (COX)-2. S1P stimulated extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) in HAC, and the PGE(2 )induction was abrogated by PD98059 and SB203580. Pertussis toxin inhibited the PGE(2 )induction from HAC by S1P, suggesting an essential role for Gi protein. S1P also attenuated the expression of proteoglycan aggrecan, a component of cartilage matrix, in HAC at transcriptional level. CONCLUSION: It was suggested that the S1P-induced PGE(2 )was at least in part involved in the aggrecan-suppressing effect of S1P, seeing as COX inhibitors attenuated the effect. Accordingly, S1P might play an important role in cartilage degradation in arthritides

A randomized, open-label comparison of once-weekly insulin icodec titration strategies versus once-daily insulin glargine u100

OBJECTIVE Insulin icodec is a novel once-weekly basal insulin analog. This trial investigated the efficacy and safety of icodec using different once-weekly titration algorithms. RESEARCH DESIGN AND METHODS This was a phase 2, randomized, open-label, 16-week, treat-to-target study. Insulin-naive adults (n = 205) with type 2 diabetes and HbA1c 7–10% while treated with oral glucose-lowering medications initiated once-weekly icodec titrations A (prebreakfast self-measured blood glucose target 80–130 mg/dL; adjustment ±21 units/week; n = 51), B (80–130 mg/dL; ±28 units/week; n = 51), or C (70–108 mg/dL; ±28 units/week; n = 52), or once-daily insulin glargine 100 units/mL (IGlar U100) (80–130 mg/dL; ±4 units/day; n = 51), all titrated weekly. Percentage of time in range (TIR) (70–180 mg/dL) during weeks 15 and 16 was measured using continuous glucose monitoring. RESULTS TIR improved from baseline (means: A, 57.0%;B,55.2%;C,51.0%; IGlar U100, 55.3%) to weeks 15 and 16 (estimated mean: A, 76.6%; B,83.0%; C,80.9%; IGlar U100, 75.9%). TIR was greater for titration B than for IGlar U100 (estimated treatment difference 7.08%-points; 95% CI 2.12 to 12.04; P = 0.005). No unexpected safety signals were observed. Level 2 hypoglycemia (<54 mg/dL) was low in all groups (0.05, 0.15, 0.38, 0.00 events per patient-year of exposure for icodec titrations A, B, and C and IGlar U100, respectively), with no episodes of severe hypoglycemia. CONCLUSIONS Once-weekly icodec was efficacious and well tolerated across all three titration algorithms investigated. The results for icodec titration A (80–130 mg/dL; ±21 units/week) displayed the best balance between glycemic control and risk of hypoglycemia